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CNS Drug Action in Neurodegenerative Diseases 3.0
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CNS Drug Action in Neurodegenerative Diseases 3.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 2846

Special Issue Editor

Prof. Dr. Stefanie Kuerten

E-Mail Website
Guest Editor
Institute of Neuroanatomy, Faculty of Medicine, University of Bonn, 53115 Bonn, Germany
Interests: autoimmunity; autoantibodies; B cells; EAE; multiple sclerosis; neuroprotection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Amyotrophic lateral sclerosis, multiple sclerosis, Alzheimer’s, and Parkinson’s disease are neurodegenerative diseases of the central nervous system, which represent a major socioeconomic burden to society. All of these diseases are similar in that their etiology is still unclear and there are different theories on their pathogenesis. While most drugs that are approved to treat neurodegeneration are able to reduce clinical symptoms and slow down disease progression, they cannot cure the disease. In addition, the availability of suitable biomarkers that could predict treatment success is very limited, so that patient-oriented therapy has remained a future goal. Yet, intensive research is ongoing to eventually unravel the mechanisms underlying neurodegeneration and central nervous system repair. This open-access Special Issue will bring together original research and review articles on the mode of action of different drugs that were designed to limit neurodegeneration, support neuroprotection, and/or to promote neural repair, highlighting what has already been achieved and which new discoveries, approaches, and technical developments in central nervous system research are on their way.

Topics of this Special Issue include but are not limited to:

  • Etiology and pathogenesis of neurodegenerative diseases;
  • Mechanisms of neurodegeneration, neuroprotection, and neural repair in the central nervous system;
  • Pharmaceutical and pharmacological central nervous system drug classification;
  • Mode of action of central nervous system drugs;
  • Past and ongoing clinical trials using CNS drugs in neurodegenerative diseases;
  • Novel strategies for the prevention and treatment of CNS degeneration.

Prof. Dr. Stefanie Kuerten
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • CNS drugs
  • neurodegenerative diseases
  • neuroprotection
  • neuroregeneration
  • pharmacology

Published Papers (2 papers)

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Research

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18 pages, 2701 KiB  
Article
Significance of Astragaloside IV from the Roots of Astragalus mongholicus as an Acetylcholinesterase Inhibitor—From the Computational and Biomimetic Analyses to the In Vitro and In Vivo Studies of Safety
by Katarzyna Stępnik, Wirginia Kukula-Koch, Wojciech Plazinski, Kinga Gawel, Katarzyna Gaweł-Bęben, Daariimaa Khurelbat and Anna Boguszewska-Czubara
Int. J. Mol. Sci. 2023, 24(11), 9152; https://doi.org/10.3390/ijms24119152 - 23 May 2023
Cited by 5 | Viewed by 1440
Abstract
The main aim of the study was to assess the acetylcholinesterase-inhibitory potential of triterpenoid saponins (astragalosides) found in the roots of Astragalus mongholicus. For this purpose, the TLC bioautography method was applied and then the IC50 values were calculated for astragalosides [...] Read more.
The main aim of the study was to assess the acetylcholinesterase-inhibitory potential of triterpenoid saponins (astragalosides) found in the roots of Astragalus mongholicus. For this purpose, the TLC bioautography method was applied and then the IC50 values were calculated for astragalosides II, III and IV (5.9 μM; 4.2 μM, and 4.0 μM, respectively). Moreover, molecular dynamics simulations were carried outto assess the affinity of the tested compounds for POPC and POPG-containing lipid bilayers, which in this case are the models of the blood-brain barrier (BBB). All determined free energy profiles confirmed that astragalosides exhibit great affinity for the lipid bilayer. A good correlation was obtained when comparing the logarithm of n-octanol/water partition coefficient (logPow) lipophilicity descriptor values with the smallest values of free energy of the determined 1D profiles. The affinity for the lipid bilayers changes in the same order as the corresponding logPow values, i.e.,: I > II > III~IV. All compounds exhibit a high and also relatively similar magnitude of binding energies, varying from ca. −55 to −51 kJ/mol. Apositive correlation between the experimentally-determined IC50 values and the theoretically-predicted binding energies expressed by the correlation coefficient value equal 0.956 was observed. Full article
(This article belongs to the Special Issue CNS Drug Action in Neurodegenerative Diseases 3.0)
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Review

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14 pages, 1977 KiB  
Review
Spinocerebellar Ataxia Type 3 Pathophysiology—Implications for Translational Research and Clinical Studies
by Fabian Stahl, Bernd O. Evert, Xinyu Han, Peter Breuer and Ullrich Wüllner
Int. J. Mol. Sci. 2024, 25(7), 3984; https://doi.org/10.3390/ijms25073984 - 3 Apr 2024
Viewed by 855
Abstract
The spinocerebellar ataxias (SCA) comprise a group of inherited neurodegenerative diseases. Machado–Joseph Disease (MJD) or spinocerebellar ataxia 3 (SCA3) is the most common autosomal dominant form, caused by the expansion of CAG repeats within the ataxin-3 (ATXN3) gene. This mutation results in the [...] Read more.
The spinocerebellar ataxias (SCA) comprise a group of inherited neurodegenerative diseases. Machado–Joseph Disease (MJD) or spinocerebellar ataxia 3 (SCA3) is the most common autosomal dominant form, caused by the expansion of CAG repeats within the ataxin-3 (ATXN3) gene. This mutation results in the expression of an abnormal protein containing long polyglutamine (polyQ) stretches that confers a toxic gain of function and leads to misfolding and aggregation of ATXN3 in neurons. As a result of the neurodegenerative process, SCA3 patients are severely disabled and die prematurely. Several screening approaches, e.g., druggable genome-wide and drug library screenings have been performed, focussing on the reduction in stably overexpressed ATXN3(polyQ) protein and improvement in the resultant toxicity. Transgenic overexpression models of toxic ATXN3, however, missed potential modulators of endogenous ATXN3 regulation. In another approach to identify modifiers of endogenous ATXN3 expression using a CRISPR/Cas9-modified SK-N-SH wild-type cell line with a GFP-T2A-luciferase (LUC) cassette under the control of the endogenous ATXN3 promotor, four statins were identified as potential activators of expression. We here provide an overview of the high throughput screening approaches yet performed to find compounds or genomic modifiers of ATXN3(polyQ) toxicity in different SCA3 model organisms and cell lines to ameliorate and halt SCA3 progression in patients. Furthermore, the putative role of cholesterol in neurodegenerative diseases (NDDs) in general and SCA3 in particular is discussed. Full article
(This article belongs to the Special Issue CNS Drug Action in Neurodegenerative Diseases 3.0)
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